1. Cell Biology
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The unfolded protein response is required for dendrite morphogenesis

  1. Xing Wei
  2. Audrey S Howell
  3. Xintong Dong
  4. Caitlin A Taylor
  5. Roshni C Cooper
  6. Jianqi Zhang
  7. Wei Zou
  8. David R Sherwood
  9. Kang Shen  Is a corresponding author
  1. Howard Hughes Medical Institute, Stanford University, United States
  2. University of Southern California, United Kingdom
  3. Duke University, United States
Research Article
  • Cited 26
  • Views 3,250
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Cite this article as: eLife 2015;4:e06963 doi: 10.7554/eLife.06963

Abstract

Precise patterning of dendritic fields is essential for the formation and function of neuronal circuits. During development, dendrites acquire their morphology by exuberant branching. How neurons cope with the increased load of protein production required for this rapid growth is poorly understood. Here we show that the physiological unfolded protein response (UPR) is induced in the highly branched Caenorhabditis elegans sensory neuron PVD during dendrite morphogenesis. Perturbation of the IRE1 arm of the UPR pathway causes loss of dendritic branches, a phenotype that can be rescued by overexpression of the ER chaperone HSP-4 (a homologue of mammalian BiP/ grp78). Surprisingly, a single transmembrane leucine-rich repeat (LRR) protein, DMA-1, plays a major role in the induction of the UPR and the dendritic phenotype in the UPR mutants. These findings reveal a significant role for the physiological UPR in the maintenance of ER homeostasis during morphogenesis of large dendritic arbors.

Article and author information

Author details

  1. Xing Wei

    Department of Biology, Howard Hughes Medical Institute, Stanford University, Stanford, United States
    Competing interests
    No competing interests declared.

  2. Audrey S Howell

    Department of Biology, Howard Hughes Medical Institute, Stanford University, Stanford, United States
    Competing interests
    No competing interests declared.

  3. Xintong Dong

    Department of Biology, Howard Hughes Medical Institute, Stanford University, Stanford, United States
    Competing interests
    No competing interests declared.

  4. Caitlin A Taylor

    Department of Biology, Howard Hughes Medical Institute, Stanford University, Stanford, United States
    Competing interests
    No competing interests declared.

  5. Roshni C Cooper

    Department of Biology, Howard Hughes Medical Institute, Stanford University, Stanford, United States
    Competing interests
    No competing interests declared.

  6. Jianqi Zhang

    Division of Biostatistics, Department of Preventive Medicine, University of Southern California, Los Angeles, United Kingdom
    Competing interests
    No competing interests declared.

  7. Wei Zou

    Department of Biology, Duke University, Durham, United States
    Competing interests
    No competing interests declared.

  8. David R Sherwood

    Department of Biology, Duke University, Durham, United States
    Competing interests
    No competing interests declared.

  9. Kang Shen

    Department of Biology, Howard Hughes Medical Institute, Stanford University, Stanford, United States
    For correspondence
    kangshen@stanford.edu
    Competing interests
    Kang Shen, Reviewing editor, eLife.

Reviewing Editor

  1. Graeme W Davis, University of California, San Francisco, United States

Publication history

  1. Received: February 11, 2015
  2. Accepted: June 7, 2015
  3. Accepted Manuscript published: June 8, 2015 (version 1)
  4. Version of Record published: June 29, 2015 (version 2)

Copyright

© 2015, Wei et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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